Sedation caused by clonidine in patients with spinal cord injury

Background. In patients with spinal cord injury, cephalad spreadof intrathecal (i.t.) medication could be delayed. Methods. We used bispectral index and an observer scale to assesssedation after two different doses of i.t. clonidine in patientswith or without spinal cord injury. Twelve patients with neurologicaldeficit caused by trauma (Spinal Cord Injury, SCI) were comparedwith patients without neurological disease. They received 10mg of i.t. bupivacaine with clonidine, with either 50 µg(low dose, n=6) or 150 µg (high dose, n=6) at L₂–L₃.A further 12 patients, six with spinal trauma lesion and sixhealthy, received i.t. bupivacaine and 150 µg of i.m.clonidine. Results. Sedation and a decrease in BIS occurred only in patientsreceiving 150 µg of clonidine. Onset of sedation and thedecrease in BIS was delayed in most spinal cord injured patientswhatever the route of administration (P<0.001). Durationof sedation was not different between the groups. Delayed sedationand decrease of BIS after i.t. clonidine in patients with spinalcord injury are similar than those observed after i.m. clonidine. Conclusion. A systemic effect is likely to be the main reasonfor sedation. Br J Anaesth 2003; 90: 742–5